Doe the climate direct mutations towards the ATP6 gene?

... the reason I brought this up is that, if there is some
suspicion over the validity of the 'mitochondrial clock' then
your argument here is non-existent.You are saying that with a 1 in 300-600 gen. mutation rate
we couldn't see what we see without NRM's, but that that
assumed rate is incorrect and in reality much faster.In which case we could explain what we observe (if we can diverge
from chimps in 150ky then the minor divergences amongst humans
is easy to accomodate).Taking assumptions from different models is a fairly easy way to
make something look impossible.PB: As you can see clearly now evolutionism messed up biology. As a result we do not understand anything anymore since all data have been subjected, corrected and normalized according to a false paradigm. Time to have an objective reanalysis of life and clean up the mess left by evolutionism.Best wishes,
peter

The other main points about the cited mutation rates
which has a bearing is that the 1 in 300-600 is based
upon the 'noise' (if you like) in the sequence.That is the unselected regions.The region that you are referring to is undergoing selection
and so the rate is invalid.Perhaps considerations along these lines are why the disparity appears
to exist.Over long periods the 1 in 300 may be valid since one may
assume (perhaps wrongly admittedly) that the noise would
predominate.Over shorter periods the selected region changes may be more noticeable if we happen to hit upon a sample set where the
changes are being forged.... I agree in a certain sense though, in that if something is not
yet understood it cannot be used as the basis for further
evidence.

dear Peter,PW: The other main points about the cited mutation rates
which has a bearing is that the 1 in 300-600 is based
upon the 'noise' (if you like) in the sequence.
That is the unselected regions.PB: How do you know that they are unselected regions? Do you know the function of this region. I bet they have a function, since the mt is so compact that even some genes demonstrate overlap. That tells me that all embellishment in the mtDNA is already got rid of.PW: The region that you are referring to is undergoing selection
and so the rate is invalid.PB: The genes I referred to undergo selection? What kind of selection? Neutral selection? These are socalled NRM. You better get used to that term.
[added by edit:] The discussion of the paper even demonstrates that some of the mutations reduce vertility in man (diminished sperm production), so in fact there would be selection AGAINST these mutations. It is evidence for my opinion: NRM.PW: Perhaps considerations along these lines are why the disparity appears to exist. Over long periods the 1 in 300 may be valid since one may assume (perhaps wrongly admittedly) that the noise would
predominate.PB: Yes, by the false paradigm of evolutionism and the addition of one chimp to a human analysis.PW: Over shorter periods the selected region changes may be more noticeable if we happen to hit upon a sample set where the
changes are being forged.PB: Than you also have to agree on the Non-random character of these mutations.PW: ... I agree in a certain sense though, in that if something is not
yet understood it cannot be used as the basis for further
evidence.PB: Great, you just objected to Dawkins nonsense about Junk DNA.Also for you there is a new thread on ancient mtDNA.best wishes,
Peter[This message has been edited by peter borger, 01-23-2003]

Thanks for that Quetzal. I'll have to chew on it a bit. I may go back to "lurking", and of course I'll make sure to try to spare you any of my philosophical rants!A quick request if it is easily seen to. In another thread PB mentioned that in a post with you a link had been posted (by you?) that referenced..."certain mutations (being)/are always introduced in vivo at the same spot due to the properties of the surrounding DNA sequences and the physicochemical properties of DNA."Do you know this reference?all the best and thanks again!

Hi Judge,It was on p53 mutations. Quetzals mentioned it in one of my threads: More nonrandom mutations or Mol gen evidence for a MPG.Best wishes,
Peter

quote:

---

In which case we could explain what we observe (if we can diverge
from chimps in 150ky then the minor divergences amongst humans
is easy to accomodate

---

We cannot do this. Your 150 kya claim is based on a flawed and overly simplistic premise - namely, that a ~350 bp mt DNA locus contains more information than the entire mitochondrial and nuclear genomes combined.

dear Page,quote:
--------------------------------------------------------------------------------In which case we could explain what we observe (if we can diverge
from chimps in 150ky then the minor divergences amongst humans
is easy to accomodate
--------------------------------------------------------------------------------Page: We cannot do this. Your 150 kya claim is based on a flawed and overly simplistic premise - namely, that a ~350 bp mt DNA locus contains more information than the entire mitochondrial and nuclear genomes combined.PB: Wrong. The sequences in ancient subspecies contain more information regarding mutations that your simplistic comparison of chimp and human mtDNA. It gives us information about the rate and the position where they are introduced: in the ancient subpopulations we are able to exactly follow mutations and mutation rates over a more accurate time scale. That the data don't fit with your evolutionary view is tale telling: evolutionism's conclusions based on comparison BETWEEN species are wrong.
Now we know that all info for variation is already preexistent in the genome we know that Darwin made an unwarranted extrapolation with respect to microbe to man evolution. If you take the contemporary observation on variation preexisting in the genomes as the mechanism that drives evolution from microbe to man (as Darwin did), than you talk about a mechanistically determined evolution, in other words creation.Best wishes,
Peter[This message has been edited by peter borger, 01-26-2003]

Hi Judge:Sorry, it took a bit of digging for me to track down which post that was. It was this post in a thread on hotspots. The post references three articles that, basically, describe "hotspots" in relation to DNA's susceptibility of a particular mutagen causing a particular mutation at a given locus. Again, it's primarily due to structure/composition. And again, hotspots can only be said to be "more likely" rather than "non-random" - IOW, a statistical increase in probability, not a guarantee. Which, of course, is why Peter has been unable to use his knowledge of molecular biology to actually predict where the next mutation will occur. Mutagens act on the whole genome - some bits of the genome are more susceptible to particular mutations than other bits. That's all.

Thank you!...as i said i have a bit of chewing to do!

dear Quetzal,Q: Sorry, it took a bit of digging for me to track down which post that was. It was this post in a thread on hotspots. The post references three articles that, basically, describe "hotspots" in relation to DNA's susceptibility of a particular mutagen causing a particular mutation at a given locus. Again, it's primarily due to structure/composition. And again, hotspots can only be said to be "more likely" rather than "non-random" - IOW, a statistical increase in probability, not a guarantee. Which, of course, is why Peter has been unable to use his knowledge of molecular biology to actually predict where the next mutation will occur.
Mutagens act on the whole genome - some bits of the genome are more susceptible to particular mutations than other bits. That's all.PB: You also like to compare apples and oranges. The mechanism that induce variation are preexistent in the genome as clearly demonstrated by contemporary molecular biology. Why don't you ask Dr Caporale for a copy of her book. Or go to a library. Listen Quetzal, it is known that oxidative stress, UV and probably mutagens induce mutations randomly. (for mutagens I would actually not be sure, since usually such chemicals can specifically interact with DNA). However, there are also mechanisms in the genome that introduce variation through NRM. You cannot compare these mechanism!If you has read the article on p53, you would have known that the mutations were dependent upon the sequence. I will look up a review for you on NRM in proto-oncogenes. Maybe that will convince you.
In the meantime, keep comparing these unequal phenomena. Very scientific.Best wishes,
Peter

Peter, a quick question. You have argued here that sequence similarity can be explained by mutations that are non random WRT position and nucleotide (or perhaps semi-random WRT nucleotide)
That mutations are non random WRT position seems clear, can you direct me to evidence that they are non random WRT nucleotide? It may be staring me in the face here somewhere as I do get a bit lost with the technical details and jargon at times.
I have just purchased Dr Caporales' book and I noticed on p.41 she argues for non randomness WRT position, but does she also argue somewhere for non randomness WRT nucleotide?It may be here on another thread perhaps?[This message has been edited by judge, 01-27-2003]

Hi Judge,On page 36-38 Dr caporale deomonstrated how such mutations can be explained. She shows a figure for the hairpin model in T4 virus (unpublished as I understood it). It explains for this stretch of DNA how the observed mutations are usually of the same nucleotide and always on the same position. Furthermore, there are studies on hotspots demonstrating such mechanism. I've mentioned a couple of them in my communication with Quetzal. I will look them up.Best wishes,
Peter

You need to re-read my post. I wasn't comparing anything. I merely stated that you had been utterly incapable of demonstrating your non-random mutation scenario. If prediction is not a part of your evidence, then what is? Your say so? As far as the mutagens go, they DO in large measure have random effects but are statistically more likely to induce mutations at particular loci. It is beyond me why a self-vaunted molecular biology expert can't understand this simple concept.As to Dr. Caporale's book, from the excerpts and links that have been posted here, it appears that at the least she has provided a good argument for the structural mechanisms behind "hotspots" - those statistically more likely mutation loci. If I'm not mistaken, she discusses the adaptive value of these spots. It sounds like a forward step in the debate over the "evolution of mutability", as she's describing the actual mechanisms for this. Here's her writing on this subject (not from the book, which I don't have, but rather from one of her papers):

quote:

---

Genomes that encode "better" amino acid sequences are at a selective advantage. Genomes that generate diversity also are at an advantage to the extent that they can navigate efficiently through the space of possible sequence changes. Biochemical systems that tend to increase the ratio of useful to destructive genetic change may harness preexisting information (horizontal gene transfer, DNA translocation and/or DNA duplication), focus the location, timing, and extent of genetic change, adjust the dynamic range of a gene's activity, and/or sample regulatory connections between sites distributed across the genome. Rejecting entirely random genetic variation as the substrate of genome evolution is not a refutation, but rather provides a deeper understanding, of the theory of natural selection of Darwin and Wallace. The fittest molecular strategies survive, along with descendants of the genomes that encode them. Caporale, LH, "Chance Favors the Prepared Genome", Annals of the New York Academy of Sciences 870:1-21 (1999)

---

Her idea is certainly well-supported, so I don't have any problem with what she is discussing. Unlike you, I'm not unfamiliar with the concepts. Here's a recent article on-line for instance: Conticello SG, Gilad Y, Avidan N, Ben-Asher E, Levy Z, Fainzilber M (2001) Mechanisms for Evolving Hypervariability: The Case of Conopeptides, MolBiolEvol 18:120-131Once again, you're stretching to shoehorn a scientist's work into your "theory" by twisting and misrepresenting the research. Very scientific.post script: On the p53 paper: Does this mean you've finally actually read it? Maybe you could quote the second paragraph from the "Materials and Methods" section, just to check. The last time we discussed it, you hadn't read it - just the title and the bit of the abstract I posted (message #23 of the thread I referenced for Judge).[This message has been edited by Quetzal, 01-28-2003]

quote:

---

from Peter Borger's post
PW: The other main points about the cited mutation rates
which has a bearing is that the 1 in 300-600 is based
upon the 'noise' (if you like) in the sequence.
That is the unselected regions.

​

PB: How do you know that they are unselected regions?
Do you know the function of this region. I
bet they have a function, since the mt is so compact that even some genes demonstrate overlap. That tells me that all embellishment in the mtDNA is already got rid of.

---

I don't know that they are unselected, but that is the assumption/
claim made in the generation of the 1 in 300-600 generation
mutation rate.Whether or not something has function has no bearing on
whether or not it is selected for in any case. Selection
is to do with the relationship between function and the
environment, not the function alone.

quote:

---

from Peter Borger's post
PW: The region that you are referring to is undergoing selection
and so the rate is invalid.

​

PB: The genes I referred to undergo selection? What kind of selection? Neutral selection? These are
socalled NRM. You better get used to that term.
[added by edit:] The discussion of the paper even demonstrates that some of the mutations reduce
vertility in man (diminished sperm production), so in fact there would be selection AGAINST these
mutations. It is evidence for my opinion: NRM.

---

I don't see how this could be selected against when mtDNA is
passed on from the mother alone (with occasional leakage
from sperm tails).Whether the males reproduce or not has little impact on the
changes in mtDNA from the mother.

quote:

---

from Peter Borger's post
PW: Perhaps considerations along these lines are why the disparity appears to exist. Over long
periods the 1 in 300 may be valid since one may assume (perhaps wrongly admittedly) that the noise
would predominate.

​

PB: Yes, by the false paradigm of evolutionism and the addition of one chimp to a human analysis.

---

Surely it's statistics (or maybe stochastics) not evolutionism?The presumption is that if there is a large amount of
random change then over a prolonged period the largest part
of the observed change will be 'noise'. i.e. there is
more unselected change than selected for over a large time
span.That's just my opinion in the matter any how. It makes some
sense to me, but I'm not saying I'm right.

quote:

---

from Peter Borger's post
PW: Over shorter periods the selected region changes may be more noticeable if we happen to hit upon a sample set where the changes are being forged.

​

PB: Than you also have to agree on the Non-random character of these mutations.

---

Why?

quote:

---

from Peter Borger's post
PW: ... I agree in a certain sense though, in that if something is notyet understood it cannot be used as the basis for further evidence.

​

PB: Great, you just objected to Dawkins nonsense about Junk DNA.

​

Also for you there is a new thread on ancient mtDNA.

---

Which nonsense about junk DNA?

Hi Quetzal,You need to re-read my post. I wasn't comparing anything. I merely stated that you had been utterly incapable of demonstrating your non-random mutation scenario.PB: Dr Lynn Caporale recently published a book on the topic of NRM. So, I presume that you also deny her book. I am starting to feel a sense of pitty when I have to discuss science with with atheistic evo's and I have to try hard to understand their non-scientific approach of data. This is what Caporale has to say about new observations and denial: "This observation [of jumping genes] was greeted by much of the scientific community with what most generously might be called denial". You are one of the deniers.Q: If prediction is not a part of your evidence, then what is?PB: Where do you get this idea? The GUToB does several predictions and they all came true. That's something one cannot say for evolutionism. For instance, evolutionism predicts that genetic redundancies should have an association with gene duplication. But they don't (refered to Winzeler et al, at least a dozen times, so you should know). Evolutionism also predicts that such genes demonstrate a higher mutatition rate. But they don't. Clear case. At least for me, since I am a scientist.Q: Your say so? As far as the mutagens go, they DO in large measure have random effects but are statistically more likely to induce mutations at particular loci.PB: Yep, and such positional NRM will give the illusion of common descent.Q: It is beyond me why a self-vaunted molecular biology expert can't understand this simple concept.PB: I understand both the evolutionary and GUToB concepts. I know which one to choose. And of course it is beyond you, since you are only willing to see the evolutionary concept. Sometimes it pays to look beyond the paradigm. And if you still are under the impression that evolutionism can explain all bioloical data, then you are wasting your time on this board. (AND I TOO, sorry for the capitals)Q: As to Dr. Caporale's book, from the excerpts and links that have been posted here, it appears that at the least she has provided a good argument for the structural mechanisms behind "hotspots" - those statistically more likely mutation loci. If I'm not mistaken, she discusses the adaptive value of these spots. It sounds like a forward step in the debate over the "evolution of mutability", as she's describing the actual mechanisms for this. Here's her writing on this subject (not from the book, which I don't have, but rather from one of her papers):quote:
--------------------------------------------------------------------------------
Genomes that encode "better" amino acid sequences are at a selective advantage. Genomes that generate diversity also are at an advantage to the extent that they can navigate efficiently through the space of possible sequence changes. Biochemical systems that tend to increase the ratio of useful to destructive genetic change may harness preexisting information (horizontal gene transfer, DNA translocation and/or DNA duplication), focus the location, timing, and extent of genetic change, adjust the dynamic range of a gene's activity, and/or sample regulatory connections between sites distributed across the genome. Rejecting entirely random genetic variation as the substrate of genome evolution is not a refutation, but rather provides a deeper understanding, of the theory of natural selection of Darwin and Wallace. The fittest molecular strategies survive, along with descendants of the genomes that encode them. Caporale, LH, "Chance Favors the Prepared Genome", Annals of the New York Academy of Sciences 870:1-21 (1999)
--------------------------------------------------------------------------------Q: Her idea is certainly well-supported, so I don't have any problem with what she is discussing.PB: It is exactly the same as what I demonstrated 7 months ago in the 1G5 gene. And denied till Caporale posted her mail to this board. Now suddenly there is NRM and it is all consistent with evolutionary theory. You evo's are so easy to see through. It is almost ridiculous. It is litterally ROTFLMAO........ No, it is sad.Q: Unlike you, I'm not unfamiliar with the concepts.PB: Unlike me? Dear Quetzal, I discovered NRM in the 1G5 gene. That's what the fuss was about last year. You know this gene that changes at a neutral rate --so selection cannot be applied-- and still demonstrates mutations on exactly the same spots in distinct subpopulations.Q: Here's a recent article on-line for instance: Conticello SG, Gilad Y, Avidan N, Ben-Asher E, Levy Z, Fainzilber M (2001) Mechanisms for Evolving Hypervariability: The Case of Conopeptides, MolBiolEvol 18:120-131PB: Thanks for the reference.Q: Once again, you're stretching to shoehorn a scientist's work into your "theory" by twisting and misrepresenting the research. Very scientific.PB: Do you really want to be involved in a Page-like diatribe? I hope you won't, although accusing me of shoehorning scientists would be a nice start. Listen Quetzal, I didn't have to read Caporale's book to demonstrate NRM and how it contradicts NDT. Dr Caporale simply confirmed my claims about NRM. I think it is clear from her book that she doen't advocate NDT, either. For instance:"So, E. coli cannot randomly try every possible change and then wait for selection to capture the very best ones." [page 72]"New levels of interaction rarely arise through letter-by-letter random mutations of random DNA sequences" [page 144]In other words, NDT is dead. RIP. And that was my claim 7 months ago. And proven beyond doubt. Anyone denying it is not a scientist.Q: post script: On the p53 paper: Does this mean you've finally actually read it?PB: Yep. BTW, I like your intonation.Maybe you could quote the second paragraph from the "Materials and Methods" section, just to check.PB: To check? You are such a comediant! Wanna check the colour of my undies too, I guess.Q: The last time we discussed it, you hadn't read it - just the title and the bit of the abstract I posted (message #23 of the thread I referenced for Judge).PB: The last time we discussed you hadn't read Caporale, and you still haven't. However, let's not waste time on non-sense. Let's discuss the rapid evolution of Bt resistance in laboratory populations of insects, and field populations of major pests possessing Bt resistance genes even before the Bt cotton crop (a transgene) was planted. [SR Palumbi. The evolution explosion. p131-161. ISBN 0-393-32338-2]It is compelling evidence for NRM in a MPG (=GUToB). All information is preexisting in the genome.Evolution from microbe to man: RIP.Best wishe,
Peter